Mammalian DNA δ15N exhibits 40‰ intramolecular variation and is unresponsive to dietary protein level.

We report the first high-precision characterization of molecular and intramolecular δ(15)N of nucleosides derived from mammalian DNA. The influence of dietary protein level on brain amino acids and deoxyribonucleosides was determined to investigate whether high protein turnover would alter amino acid (15)N or (13)C values. Pregnant guinea pig dams were fed control diets, or high or low levels of dietary protein throughout gestation, and all pups were fed control diets.

Differential tissue dose responses of (n-3) and (n-6) PUFA in neonatal piglets fed docosahexaenoate and arachidonoate.

Docosahexaenoic acid (DHA) and arachidonic acid (ARA) are commonly added to infant formula worldwide; however, dietary concentrations needed to obtain optimal tissue levels have not been established. Hence, we studied tissue responses in piglets fed various doses of DHA and ARA. Doses were 0, 1, 2, and 5 times those used in U.

Long chain polyunsaturate supplementation does not induce excess lipid peroxidation of piglet tissues.

Background: Addition of highly polyunsaturated fatty acids to infant formulas raises the possibility of increased lipid peroxidation.

Aim Of The Study: We determined the effects of increasing levels of dietary docosahexaenoic acid (DHA) and arachidonic acid (AA) on lipid peroxidation and peroxidative potential in piglet tissues.

Methods: Four groups of piglets (n = 6) were bottle-fed a formula containing one of four treatments: no long chain fatty acid (Diet 0) and three different levels of DHA/AA at 1-fold (0.

Straight-chain acyl-CoA oxidase knockout mouse accumulates extremely long chain fatty acids from alpha-linolenic acid: evidence for runaway carousel-type enzyme kinetics in peroxisomal beta-oxidation diseases.

Extremely long chain polyunsaturated fatty acids (ELCPs) with >24 carbons and four or more double bonds are normally found in excitatory tissues but have no known function, and are greatly increased in brain and other tissues of humans with peroxisomal disorders. Straight-chain acyl-CoA oxidase (AOX) catalyzes the first, rate-limiting step of peroxisomal beta-oxidation of very-long-chain saturated and unsaturated fatty acids. We have studied the polyunsaturated fatty acid metabolism of AOX knockout mice (AOX-/- as a model of human AOX deficiency (pseudo-neonatal adrenoleukodystrophy), and as a genetic tool to test the putative peroxisomal beta-oxidation involvement in polyunsaturated fatty acid synthesis.